1. Neonatal physiological pathology Flashcards
What form of jaundice is common and not concerning in neonates?
-Physiological jaundice - children are well and normally occurs between 2-14 days
-50% of term babies develop jaundice
-Jaundice in first 24h of life is NEVER NORMAL and should be investigated
What should you be concerned about if jaundice develops in the first 24h of life?
UNCONJUGATED
-Haemolytic disease
-Sepsis
-Genetic / metabolic (G6PD deficiency, hereditary spherocytosis)
CONJUGATED
-Congenital infections
-Neonatal hepatitis
What should you be concerned about if jaundice is present after 14 days?
UNCONJUGATED
-Breast milk jaundice (resolves within 3-4 weeks)
-Sepsis
-Hypothyroidism
-Excess haemolysis, bruising, polycythaemia
CONJUGATED
-Biliary atresia
-Neonatal hepatitis
-TORCH, CF
What can cause conjugated jaundice and what are the features?
FEATURES
-Clay-coloured stools
CAUSES
-Usually due to neonatal liver disease
-Congenital infections eg TORCH
-Biliary atresia (absence of biliary tree) –> no bile –> cannot break down fat –> no absorption of vit K –> bleeding
-Neonatal hepatitis (TPN / drugs)
-CF
-Metabolic disorders
What investigations should you order for a child with neonatal jaundice?
Depends on duration of symptoms
1. Direct Coombs test (if +ve –> haemolytic disease of newborn)
2. Maternal and foetal blood group (ABO Rh incompatibility)
3. Bilirubin level + direct bilirubin
-Infection / septic screen
-Platelets (thrombocytopenia)
-Reticulocytes (if high –> haemolysis)
-TFTs
-G6PD status
-LFTs (conj and unconj bili)
-Urine
How should you manage significant jaundice?
-Adequate hydration through good feeding (incl breast)
-Treat underlying cause
-Blue light phototherapy
–Breaks down bilirubin into a water soluble form that can be excreted into urine, can stop treatment once bilirubin falls 50 below treatment line
-Exchange blood transfusion (if bilirubin v high)
–Treatment threshold used to decipher whether phototherapy or exchange transfusion is necessary
What complications can occur in extreme hyperbilirubinaemia?
Kernicterus - dystonic cerebral palsy
-Unconjugated bilirubin collects in basal ganglia
What is haemolytic disease?
-Haemorrhage of foetal blood of differing rhesus group into the maternal circulation
–Leads to anti-D IgG production
–Usually foetus is RhD +ve and mother is RhD -ve
-Antibody passes into foetal circulation causing foetal RBC haemolysis
-Condition is asymptomatic / mild in first affected pregnancies, with subsequent pregnancies increasing in severity
-Effect seen once baby is born as own immune system takes over
How does haemolytic disease cause neonatal jaundice?
-Baby makes more RBCs very quickly to combat haemolysis
-As RBCs break down, bilirubin is formed that cannot be easily excreted
What risk factors are there for haemolytic disease?
-Amniocentesis
-Maternal haemorrhage
How does haemolytic disease present (antenatal vs postnatal vs late)?
ANTENATAL
-Foetal anaemia
-Bilirubin in amniotic fluids
-Foetal hepatosplenomegaly
-Hydrops foetalis (fluid accumulation in 2+ compartments eg ascites, pleural / pericardial effusion)
POSTNATAL
-Hydrops foetalis
-Bilirubinaemia / early jaundice / kernicterus
-Cutaneous haemopoietic lesions
-Hepatosplenomegaly
-Coagulopathy
-Thrombocytopenia / leukopenia
LATE
-Anaemia
-Inspissated bile syndrome
What investigations would you order for haemolytic disease?
-Maternal blood - group, Anti Rh
-Cord / neonatal blood
–Low Hb?
–High reticulocytes?
–Low platelets?
–DCT +ve
–Raised serum bilirubin?
How should you manage haemolytic disease?
-Close supervision + ?intrauterine blood transfusion
-If anticipated to be severe have O neg blood available at delivery
-After birth:
–Check HR
–Start high risk infants on phototherapy
–Consider IV Ig therapy
-Blood transfusion if anaemia is severe
-Correct coagulopathies
-Oral folic acid for 6 months
PROPHYLAXIS
-Rh anti-D IgG given to a RhD -ve mother at 28 weeks and after birth of Rh +ve foetus
What is respiratory distress syndrome in neonates?
-Lung disease caused by surfactant deficiency
-Produced from week 30 so largely seen in preterm infants (type II pneumocytes develop form week 24)
-Surfactant deficiency causes alveolar collapse –> increased work of breathing and hypoxia due to shunting
What is the normal disease pattern of RDS?
-If untreated - disease worsens over 48-72h
-Depending on severity, resolves over 5-7 days
-Mortality is 5-10% depending on severity and gestation
